EFFECTS OF PROLONGED BLOCKADE OF THE RENIN-ANGIOTENSIN SYSTEM ON STRIATED-MUSCLE MICROCIRCULATION OF SPONTANEOUSLY HYPERTENSIVE RATS

Citation
Kj. Scheidegger et al., EFFECTS OF PROLONGED BLOCKADE OF THE RENIN-ANGIOTENSIN SYSTEM ON STRIATED-MUSCLE MICROCIRCULATION OF SPONTANEOUSLY HYPERTENSIVE RATS, The Journal of pharmacology and experimental therapeutics, 278(3), 1996, pp. 1276-1281
Citations number
35
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00223565
Volume
278
Issue
3
Year of publication
1996
Pages
1276 - 1281
Database
ISI
SICI code
0022-3565(1996)278:3<1276:EOPBOT>2.0.ZU;2-Z
Abstract
Changes in microcirculation play an important role in the pathogenesis and maintenance of hypertension. The changes can be due to an alterat ion in vessel diameter or in the number of small blood vessels. In thi s study, the effects of prolonged administration of different blockers of the renin angiotensin system on the microcirculation of the cutane ous maximus muscle of young spontaneously hypertensive rats were deter mined by using the dorsal microcirculatory chamber model. Animals were treated with the angiotensin-converting enzyme inhibitor (ACE inhibit or) benazeprilat (3 mg/kg/d) or the specific angiotensin II AT(1) rece ptor antagonist valsartan (3 mg/kg/d) for 4 weeks. Blood pressure was significantly lowered by 22 to 33% and to a similar extent in both tre atment groups, whereas blood pressure in the control group continued t o rise. Microvascular diameters and density were measured before and d uring the drug treatment and compared with those in the control group. There was no significant effect of either of the drug treatments on v ascular diameters when compared with the control group for any vessel type (arterioles or venules),ln contrast, there was a significant decr ease in small arteriolar and venular density and in large venular dens ity after treatment with the ACE inhibitor, whereas the angiotensin II AT(1) receptor antagonist had no significant effect. The data do not suggest a role for angiotensin II in the long-term control of striated muscle microvascular tone. However, angiotensin II may be involved in microvascular growth via a non-AT(1) receptor-mediated mechanism, or other vasoactive peptides degraded by ACE may contribute to the effect s of the ACE inhibitor.